MT2A and endothelial dysfunction: Although the particles clearly induce pathways relevant to endothelial dysfunction (ET-1), carcinogenicity (CYP1A1), and metal toxicity (metallothionein-II), the exposures did not measurably initiate inflammation (wildtype) or exacerbate existing inflammation (TNF) in the lungs as measured by lavage cytology and global pulmonary gene expression.